• K Przyklenk, A Aoki, S Bellows, D Klinedinst, P Zubiate, S L Hale, B Z Simkhovich, R A Kloner, and G L Kay.
• Heart Institute, Hospital of the Good Samaritan, Los Angeles, CA 90017-2395.
• J Card Surg. 1994 May 1; 9 (3 Suppl): 506-16.

Abstract"Stunned myocardium" is defined as the prolonged but transient postischemic contractile dysfunction of viable myocardium that has been salvaged by reperfusion. This phenomenon, although first characterized in the experimental canine model of coronary artery occlusion/reperfusion, also occurs following transient global ischemia. Moreover, despite the superb cardioprotection conferred by administration of cold cardioplegia during aortic cross-clamping, stunned myocardium is a well-recognized sequela of prolonged cardiopulmonary bypass. Using the anesthetized open chest dog, we tested the concept that continuous retrograde infusion of warm blood cardioplegia would effectively prevent ischemia during prolonged aortic cross-clamping and thereby preclude the development of stunned myocardium following bypass. Thirteen dogs were placed on cardiopulmonary bypass and randomized to receive: (1) continuous retrograde administration of warm blood cardioplegia (n = 8); or (2) intermittent retrograde cold blood cardioplegia (n = 5) during a 3-hour cross-clamp period. Left ventricular (LV) systolic function (i.e., area LV ejection fraction and posterior LV free wall thickening assessed by two-dimensional echocardiography) and hemodynamic parameters were monitored at baseline and at 1 and 2 hours postbypass and, at the end of the protocol, transmural myocardial biopsies were obtained for electron microscopic analysis. All dogs in both treatment groups showed electron microscopic evidence of mild and reversible morphological injury indicative of stunned myocardium, with no difference between dogs that received warm versus cold cardioplegia. Direct comparison of LV function between the two groups was confounded by a profound decrease in afterload in dogs that received cold cardioplegia. However, incorporation of systemic vascular resistance as a covariate revealed that LV function following bypass was modestly depressed at approximately 85% of baseline values, and that continuous administration of warm cardioplegia did not prevent this hypokinesis. Thus, in our canine model: (1) morphological injury and LV dysfunction induced by 3 hours of aortic cross-clamping is subtle; and (2) continuous retrograde infusion of warm blood cardioplegia during the cross-clamp period failed to preclude myocardial stunning following prolonged cardiopulmonary bypass.

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